alexa Liposomal N-acetylcysteine Modulates the Pathogenesis of P. aeruginosa Isolated from the Lungs of Cystic Fibrosis Patient | OMICS International | Abstract
ISSN: 2157-7439

Journal of Nanomedicine & Nanotechnology
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Research Article

Liposomal N-acetylcysteine Modulates the Pathogenesis of P. aeruginosa Isolated from the Lungs of Cystic Fibrosis Patient

Ahad Hasanin and Abdelwahab Omri*

The Novel Drug & Vaccine Delivery Systems Facility, Department of Chemistry and Biochemistry, Laurentian University, Sudbury, ON, P3E 2C6, Canada

*Corresponding Author:
Abdelwahab Omri
The Novel Drug & Vaccine Delivery Systems Facility
Department of Chemistry and Biochemistry
Laurentian University, Sudbury, ON, P3E 2C6, Canada
Tel: +1-705-675-1151, ext. 2190
Fax: +1-705675-4844
E-mail: [email protected]

Received Date: July 25, 2014; Accepted Date: August 21, 2014; Published Date: August 27, 2014

Citation: Hasanin A, Omri A (2014) Liposomal N-acetylcysteine Modulates the Pathogenesis of P. aeruginosa Isolated from the Lungs of Cystic Fibrosis Patient. J Nanomed Nanotechnol 5:219 doi:10.4172/2157-7439.1000219

Copyright: © 2014 Hasanin A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

N-acetylcysteine (NAC) is a mucolytic agent with antimicrobial potential. We evaluated the antimicrobial activity of the free and liposomal NAC (F-NAC; L-NAC) against Pseudomonas aeruginosa. The minimum inhibitory concentrations (MIC), the minimum bactericidal concentrations (MBC) and the in vitro time kill studies of L-NAC were determined by broth-dilution method. Efficacy of the formulations on the production of N-acyl homoserine lactone molecules, virulence factors and motility were determined. Eradication of bacterial community within biofilms was assessed using the Calgary Biofilm Device. The L-NAC Cytotoxicity and anti-bacterial adhesion potential to human lung cells were examined using pulmonary A549 cell lines. The MIC of L-NAC was lower than the free drug (1250 mg/L and 5000 mg/L, respectively). MBC for L-NAC was 2500 mg/L compared to 5000 mg/L for F-NAC. L-NAC at 2500 mg/L killed bacteria in 2 h, whereas F-NAC exhibited the same effect at 5000 mg/L. Quorum sensing was significantly inhibited by L-NAC (P<0.001). At 1/8 MIC, L-NAC reduced the production of bacterial proteases significantly more than that of F-NAC at 1/4 MIC. L-NAC was also able to reduce the bacterial motility at eightfold lower concentration than F-NAC (P<0.001). As for biofilms, L-NAC provided 75% protection against biofilm formation, 90% reduction in the formed biofilms, and a 46% eradication effect on bacterial community within biofilms compared to treated biofilm with PBS (P<0.001). Finally, L-NAC at 2500 mg/L was safe to A549 cells, reduced bacterial adhesion by 15% compared to control (P<0.001). These data indicate that L-NAC formulation is more effective than F-NAC against P. aeruginosa and has the potential to improve therapeutic outcomes in CF patient.

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